Stress, 2011; Early Online: 1–8
q Informa Healthcare USA, Inc.
ISSN 1025-3890 print/ISSN 1607-8888 online
DOI: 10.3109/10253890.2011.594121
Prenatal maternal anxiety and early childhood temperament
MEGAN M. BLAIR1, LAURA M. GLYNN1,3, CURT A. SANDMAN1, & ELYSIA POGGI DAVIS1,2
1
Department of Psychiatry & Human Behavior, University of California, Irvine, Orange, CA, USA, 2Department of
Pediatrics, University of California, Irvine, CA, USA, and 3Crean School of Health and Life Sciences, Chapman University,
Orange, CA, USA
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(Received 28 December 2010; revised 29 March 2011; accepted 1 June 2011)
Abstract
The consequences of exposure to prenatal maternal anxiety for the development of child temperament were examined in a
sample of 120 healthy, 2-year-old children. Prenatal maternal state and pregnancy-specific anxiety (PSA) were measured five
times during pregnancy, and maternal state anxiety was measured again at 2 years post partum. Child temperament was
measured at 2 years using the Early Childhood Behavior Questionnaire. The relationship between the trajectory of maternal
anxiety across gestation and negative affectivity was evaluated using hierarchical linear growth curve modeling. Higher
maternal PSA between 13 and 17 weeks of gestation was associated with increased negative temperament in the children. This
association could not be explained by postnatal maternal anxiety, demographic, or obstetric factors. Prenatal maternal state
anxiety was not associated with child temperament. These findings demonstrate that PSA early in gestation has a distinctive
influence on the developing fetus.
Keywords: Anxiety, child development, fetal programing, pregnancy, pregnancy-specific anxiety, temperament
Introduction
The prenatal period is a time of rapid development
during which the fetus is especially vulnerable to both
positive and negative influences that can have lasting
consequences on development across the lifespan.
These influences on the fetus have been described as
programing: the process by which an insult or
stimulus during a sensitive developmental period has
a long-lasting or permanent effect (Barker 1998).
Fetal organs and organ systems develop rapidly in a
specific sequence during gestation and go through
distinct periods of rapid cell division (Creasy and
Resnik 1994; Cameron and Demerath 2002). During
these periods of rapid cell division, organs are
especially vulnerable to environmental influences
such as stress (Kajantie 2006). Thus, the developmental consequences are dependent on both the level
and timing of exposure to environmental stimuli
during gestation (Sandman and Davis 2010). The
goal of the current study was to explore the influence
of prenatal maternal anxiety on the development of
child temperament and to investigate whether there
were timing effects of exposure to prenatal anxiety on
child outcome.
Maternal stress during pregnancy shortens the
length of gestation and threatens the developing fetal
nervous system. In humans, it has been clearly
documented that prenatal stress is associated with
preterm delivery (Copper et al. 1996; Glynn et al.
2001, 2008; Dole et al. 2003; Hobel and Culhane
2003), but less is known about the impact of prenatal
maternal psychological state on child behavioral and
psychological development. A collection of evidence
from animal studies demonstrates that exposure to
prenatal stress can alter the neurobiology and behavior
of the offspring. Prenatal exposure to maternal stress is
associated with fearful and depressive-like behaviors,
reduced social drive and more abnormal social
behavior, increased stress reactivity, and more irritable
temperament in both rodents and non-human
primates (Schneider 1992; Clarke and Schneider
1993; Clarke et al. 1994; Griffin et al. 2003;
Dickerson et al. 2005; Van den Hove et al. 2005;
Abe et al. 2007; Lee et al. 2007). These findings
Correspondence: E. P. Davis, Department of Psychiatry & Human Behavior, University of California, 333 City Boulevard West, Suite 1200,
Orange, CA 92868, USA. Tel: 1 (714) 940 1924. Fax: 1 (714) 940 1939. E-mail: [email protected]
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2
M. M. Blair et al.
indicate that prenatal stress exerts an influence on fetal
neurodevelopment. However, vast interspecies differences in both developmental trajectories and maternal
stress and reproductive physiology limit the ability to
generalize from animals to humans.
Accumulating evidence from human studies has
shown that maternal stress during pregnancy exerts
persisting influences on human development. Children exposed to prenatal maternal psychological
distress maybe particularly vulnerable to increases in
fearful or reactive behavior and difficult temperament
during infancy and toddlerhood (Huizink et al. 2002;
Davis et al. 2004, 2007; Austin et al. 2005; Gutteling
et al. 2005; Bergman et al. 2007). These early
temperament and emotional difficulties appear to
persist and result in increases in behavioral problems
during childhood (O’Connor et al. 2002; Van den
Bergh and Marcoen 2004). Importantly, these
associations are present after adjusting for postnatal
influences including postnatal maternal psychological
distress. Although compelling evidence exists for
long-lasting consequences of prenatal adversity (Van
den Bergh and Marcoen 2004; Mennes et al. 2006;
Buss et al. 2010), it is likely that aspects of the
postnatal environment including quality of maternal
care will moderate the consequences of prenatal
exposures (Bergman et al. 2008).
Thus far, most studies have focused on general
measures of prenatal maternal psychological distress
such as perceived stress, state anxiety, and depression.
However, more recent studies suggest that pregnancyspecific anxiety (PSA) maybe superior to general
measures of distress for predicting developmental
outcomes because it more accurately characterizes
psychological state specific to a woman during pregnancy
(Dunkel Schetter 2009; Sandman et al. 2011).
Concern or worry that is specific to pregnancy may
have profound implications for both birth outcome
and child development. It is only relatively recently,
however, that a woman’s fears and beliefs about
pregnancy, delivery, and health of the baby have been
investigated. This construct has been shown to be an
independent entity, separate from measures of
generalized anxiety or other psychological distress
measures (DiPietro et al. 2004; Huizink et al. 2004;
Roesch et al. 2004; Dunkel Schetter 2009). Indeed,
only a moderate amount (8 – 27%) of variance in PSA
was found to be explained by general anxiety and
depression (Huizink et al. 2004). Measures of PSA
predict a wide variety of developmental outcomes
including fetal behavior (DiPietro et al. 2002), birth
outcome (Roesch et al. 2004; Kramer et al. 2009;
Dunkel Schetter 2011), and infant and child development. Infants and toddlers exposed to elevated PSA
display poorer cognitive performance (Davis and
Sandman 2010), delayed motor development
(Huizink et al. 2003; DiPietro et al. 2006), and poor
attention regulation (Huizink et al. 2002). These early
effects appear to have consequences for the developing brain with effects that persist through childhood.
Buss et al. (2010) found that elevated PSA at the
earliest assessment (19 weeks) was associated with
focal decreases in gray matter density in several
regions, primarily in the prefrontal cortex and the
medial temporal lobe. Few longitudinal studies with
multiple prenatal assessments of PSA exist. However,
those with multiple prenatal assessments indicate that
exposure to elevated PSA early in gestation exerts a
stronger influence on infant and child development
(Huizink et al. 2002; Buitelaar et al. 2003; Buss et al.
2010; Davis and Sandman 2010).
Evaluating the link between the prenatal environment and negative or inhibited temperament in early
childhood is important because these children have a
higher risk of developing psychological disorders
including increased anxiety and depression in later life
(Kagan et al. 1999; Schwartz et al. 1999; De Pauw and
Mervielde 2010; Dougherty and Klein 2010). DiPietro
et al. (2006) reported that mothers who rated their
pregnancies as more negative than positive had children
with poorer emotional regulation and engagement/
orientation as indexed by the Bayley Scales of Infant
Development at 2 years of age (Bayley 1993). These
data indicate that pregnancy-related anxiety or concern
maybe associated with difficulty regulating emotion and
behavior. However, no study has examined the
consequences of pregnancy-related anxiety for negative
or reactive temperament during early childhood.
The aims of the current study were to determine
(i) whether prenatal maternal state anxiety and PSA
were associated with child temperament at 2 years
and (ii) whether there is a sensitive prenatal period
during which PSA exerts effects on development. We
hypothesized that psychological distress during the
prenatal period would be associated with increased
negative affectivity, PSA would exert a stronger
influence than general anxiety, and that earlier
exposures would exert a stronger influence.
Methods
Study overview
Study participants included mother– child pairs from
a longitudinal study of prenatal stress and development. Women with singleton pregnancies less than 16
weeks gestational age were recruited from obstetric
clinics in southern California and were followed
longitudinally through 2 years post partum.
Participants
The current sample included 120 full-term children
(50% first born, 45% female) and their mothers.
Initial prenatal recruitment criteria were as follows:
English speaking, over the age of 18 years, and no
Prenatal anxiety and child temperament
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steroid medication. Exclusion criteria included: use
of any recreational drugs and regular use of alcohol or
nicotine during the index pregnancy. Presence of
psychiatric problems was not an exclusion criterion;
however, in our low-risk sample, only four women had
a lifetime history of hospitalization for any emotional
problem, and only three women took antidepressant
medication during their pregnancy. In addition, all
children included in the current investigation were
full-term at birth (M gestational age ¼ 39.6 weeks,
SD ¼ 1.1 weeks). Mothers gave written informed
consent for all aspects of the protocol, which was
approved by the Institutional Review Board for
protection of human subjects. Descriptive information
for this sample is provided in Table I.
Procedures
Prenatal maternal state anxiety and PSA were collected
five times during pregnancy (Time 1: 15.5 (M) ^ 1.06
(SD); Time 2: 19.7 ^ 1.05; Time 3: 25.8 ^ 1.00;
Time 4: 31.1 ^ 0.82; Time 5: 36.8 ^ 0.78 weeks of
gestation). Maternal state anxiety and maternal report
of child temperament also were collected 2 years post
partum (M ¼ 24.1 ^ 0.39 months). Maternal state
anxiety was measured at 2 years in order to statistically
adjust both for postnatal influences on child temperament, and for reporting bias that might have occurred
when mothers rated the temperament of their children.
Demographic information was obtained through
structured interviews at each study visit. Prenatal
medical history and risk for adverse obstetric outcomes
were obtained from extensive structured medical
interviews conducted by a research nurse at each visit
in combination with a thorough review of prenatal and
hospital medical records.
Table I. Description of the study sample.
Study sample (N ¼ 120)
Maternal age at delivery (M, years)
Married or cohabitating (%)
Primiparous (%)
Education (%)
High school or equivalent
Associates or vocational
Bachelors degree
Graduate degree
Annual household income (%)
$0–$30,000
$30,001– $60,000
$60,001– $100,000
Over $100,000
Race/ethnicity (%)
Non-hispanic white
Latina
Asian
* SD ¼ 5.2, range ¼ 18–40.
30.0*
91
50
5
18
33
21
27
20
27
26
48
30
18
3
Measures
Maternal psychological assessments. The 10-item State
Anxiety subscale of the State-Trait Personality
Inventory (STAI; Spielberger 1983a) was used to
measure state, or generalized, anxiety. The STAI
assessed the degree to which participants had
experienced anxiety-related symptoms or emotions.
Responses were made using a 4-point Likert scale
ranging from 1 (not at all) to 4 (very much), and scores
could range from a minimum of 10 to a maximum of
40. The STAI has been used for research purposes
with both pregnant (Rini et al. 1999; Glynn et al.
2008) and non-pregnant samples. The STAI has good
internal consistency with a Cronbach’s a coefficient of
0.92 (Spielberger 1983b).
PSA was measured using the 10-item PregnancyRelated Anxiety scale. This measure assesses a
woman’s feelings about her health during pregnancy,
the health of her baby and her feelings about labor and
delivery. Answers were given on a 4-point Likert scale
ranging from 1 (not at all) to 4 (very much) and
included items such as: I am fearful regarding the
health of my baby, I am concerned or worried about
losing my baby, and I am concerned or worried about
developing medical problems during my pregnancy.
The final score on this measure could range from 10 to
40. This reliable measure was specifically developed
for use in pregnancy research and has good internal
consistency (a ¼ 0.75 – 0.85; Rini et al. 1999; Glynn
et al. 2008).
Child temperament. Child temperament was collected
by maternal report at 2 years of age using the Early
Child Behavior Questionnaire (ECBQ; Putnam et al.
2006). The ECBQ was developed specifically to
reduce the possibility of maternal reporting bias by
asking about specific behaviors in defined situations,
rather than asking for judgments about child
temperament or behavior. The ECBQ takes
advantage of a mother’s ability to reflect on her
child’s behavior in a wide variety of contexts. Three
broad dimensions, or factors, of temperament are
identified using the ECBQ, and published studies
have shown good internal consistency and validity for
each of these scales (Putnam et al. 2006). Because of
evidence indicating that prenatal psychological
distress is associated with increases in negative affect
and behavioral reactivity (Huizink et al. 2002;
O’Connor et al. 2002; Davis et al. 2004; Van den
Bergh and Marcoen 2004; Austin et al. 2005;
Gutteling et al. 2005; Bergman et al. 2007) and
evidence that negative temperament at ages 2 to 3 is
predictive of psychological disorders later in life
(Schwartz et al. 1999; Prior et al. 2000; Dougherty
and Klein 2010), we focused on the Negative
Affectivity subscale of the ECBQ. The Negative
Affectivity scale comprises eight subscales
4
M. M. Blair et al.
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(discomfort, fear, motor activation, sadness,
perceptual sensitivity, shyness, frustration, and
loading negatively, soothability) with Cronbach’s a
coefficients ranging from 0.73 to 0.88 (Putnam et al.
2006). Responses on the ECBQ ranged from 1 (never)
to 7 (always) and the Negative Affectivity scale
comprises items such as: when told that it was time for
bed or a nap, how often did your child get irritable;
when having trouble completing a task, how often did
your child become sad; and during everyday activities,
how often did your child startle at loud noises?
Prenatal course and birth outcome. Based on the review
of maternal medical records, a binary score assessing
the presence or absence of prenatal obstetric risk was
derived (Hobel 1982). This obstetric risk score includes
the assessment of infection, pregnancy-induced
hypertension, gestational diabetes, oligohydramnios,
polyhydramnios, preterm labor, vaginal bleeding,
placenta previa and anemia in the index pregnancy.
Data analysis
Preliminary analyses were carried out using correlations and t-tests to identify sociodemographic
(maternal race/ethnicity, maternal age, cohabitating
with child’s father, and years of maternal education),
pregnancy-related (obstetric risk, gestational age at
birth), and child (sex, birth order) variables that might
affect maternal psychological state and/or development of child temperament. Variables that were
significantly associated with negative affectivity
( p , 0.05) were maternal age at delivery, number of
years of education, race/ethnicity (Latina: 0 ¼ no,
1 ¼ yes), and cohabitating with the father of child
(0 ¼ no, 1 ¼ yes). Higher child negative affectivity
was reported by mothers who were younger
(r ¼ 2 0.29; p , 0.01), of Latina descent (t ¼ 2 2.5;
p , 0.05), had less education (r ¼ 2 0.32; p , 0.01),
and were not living with the father of the child at time
of study enrollment (t ¼ 2.5; p , 0.05). All variables
that were associated with child negative affectivity in
preliminary analyses were included as covariates in all
subsequent analyses. In addition, maternal state
anxiety at 2 years post partum was used as a covariate
in all analyses to adjust for the effects of concurrent
maternal psychological state on child temperament
and/or maternal report of temperament.
Hierarchical linear modeling (HLM) growth curve
analyses (Raudenbush and Bryk 2002; Singer and
Willett 2003) were used to describe the trajectory of
prenatal indicators of maternal anxiety (state anxiety
and PSA) across pregnancy and its association with
toddler temperament. HLM, when used with
repeated measures, treats the data in a hierarchical
fashion with observations nested within persons. This
approach allows variance to be modeled at multiple
levels and provides several advantages over ordinary
least squares regression (Raudenbush and Bryk 2002).
First, standard regression or analysis of variance
models are limited to one component of variability, the
deviation of the individual from the group mean. In
contrast, HLM includes the within-person variability
assessed over time. Second, estimates of goodness of
fit in modeling each individual’s data are derived, and
the most reliable data are given greater statistical
weight. Third, HLM produces robust estimates
despite missing values for the repeated dependent
measure. There were 110 participants who had
complete data at all prenatal assessments. Ten
participants had missing data at one prenatal visit. In
HLM models, all cases are included in the estimation
of effects, but cases with complete data are weighted
more heavily. Finally, HLM uses precise measures of
timing (i.e. gestational week) of data collection rather
than nominal estimates of assessment intervals.
Separate two-level models were constructed to
determine the association between the trajectory of
maternal anxiety across gestation and toddler negative
affectivity. A linear model was a better fit for state
anxiety. For PSA, a quadratic function was a better fit.
In both cases, predictor and outcome variables were
modeled as continuous variables. Level 1 variables, or
those evaluated longitudinally across the 5 prenatal
assessment days, included maternal state anxiety and
PSA and fetal age in weeks at the time of maternal
assessment. Negative Affectivity measured at 2 years
of age was the outcome of interest and was modeled
continuously at level 2 along with the covariates
described above. First, the overall model was tested to
determine whether temperament was significantly
associated with the intercept (set at the first
assessment, 13 gestational weeks) or the trajectory of
prenatal anxiety (linear function for state anxiety and
quadratic function for PSA). If temperament was
associated with the trajectory of pregnancy anxiety,
the model was tested centered at each gestational week
within the range of prenatal psychosocial assessments
(13 – 39 weeks of gestation) to determine whether
there was an effect of timing of exposure. The p values
of less than 0.05 were considered statistically
significant.
Results
Maternal psychological state
Significant changes were observed in the trajectory
over gestation of maternal PSA (t ¼ 3.25, b ¼ 0.001,
p , 0.01) but not state anxiety ( p ¼ 0.25). Average
levels of PSA were highest in early pregnancy and
decreased through mid-gestation. Levels of PSA
(r ¼ 0.68 –0.88) and state anxiety (r ¼ 0.49 –0.71)
were significantly correlated across pregnancy.
Significant correlations between concurrent measures
Prenatal anxiety and child temperament
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Maternal prenatal psychological state and child
temperament
Descriptive information for child temperament is
provided in Table II. Children who displayed more
negative affectivity at 2 years of age had been exposed
to higher maternal PSA early in gestation. Specifically,
negative affectivity was associated with both the initial
intercept (t ¼ 2.5; b ¼ 2.4; p , 0.05) and the trajectory across gestation of PSA (t ¼ 2.0; b ¼ 0.001;
p , 0.05). Follow-up tests to explore effects of timing
indicated that children who displayed more negative
affectivity had been exposed to higher maternal PSA
from 13 to 17 weeks of gestation (ts ¼ 2.0 – 2.4;
bs ¼ 0.16 –0.25; all p , 0.05). PSA and negative
affectivity were not significantly associated after 17
weeks of gestation (ts ¼ 0.90 – 1.86; bs ¼ 0.08 – 0.14;
all p . 0.07). Furthermore, neither level nor trajectory of state anxiety was associated with child negative
affectivity. Figure 1 displays PSA across gestation for
children scoring in the top and bottom quartiles of
negative affectivity.
Discussion
During early gestation, a mother’s fears and concerns
about her pregnancy, the health of her fetus, and her
delivery are associated with the temperament of her
child at 2 years of age. Importantly, prenatal maternal
Table II. Descriptive information (mean and SD) for prenatal and
postnatal measures.
M (SD)
Prenatal state anxiety (STAI)
15.5 ^ 1.06 wks GA
19.7 ^ 1.05 wks GA
25.8 ^ 1.00 wks GA
31.1 ^ 0.82 wks GA
36.8 ^ 0.78 wks GA
Pregnancy-specific anxiety (PSA)
15.5 ^ 1.06 wks GA
19.7 ^ 1.05 wks GA
25.8 ^ 1.00 wks GA
31.1 ^ 0.82 wks GA
36.8 ^ 0.78 wks GA
Postnatal maternal state anxiety (STAI; N ¼ 120)
Child negative affectivity (N ¼ 120)
Note: wks, weeks; GA, gestational age.
17.0(4.83)
16.7(4.48)
16.2(4.70)
16.7(5.01)
17.6(5.32)
18.6(5.40)
17.5(4.46)
17.5(4.60)
17.1(4.98)
17.6(5.23)
17.1(5.64)
2.87(0.54)
PSA with negative affectivity
22
High negative affectivity
21
Pregnancy-specific anxiety
of state anxiety and PSA were additionally observed
throughout pregnancy (average r ¼ 0.52, all
p , 0.001).
Women with elevated state anxiety (rs ¼ 0.41 – 0.61,
all p , 0.001) and PSA (rs ¼ 0.29 – 0.40, all p , 0.01)
during gestation were significantly more likely to have
elevated state anxiety during the postnatal period.
Descriptive information for pre- and postnatal
maternal psychological state can be found in Table II.
5
Low negative affectivity
20
19
18
17
16
15
14
0
15
19
25
31
36
Gestational week
Figure 1. Elevated PSA early in gestation is associated with
increased negative affectivity at 2 years of age after adjusting for
concurrent maternal anxiety and prenatal obstetric risk (all t ¼ 2.0–
2.4, b ¼ 0.16–0.25, p , 0.05). Note: Both maternal PSA and child
negative affectivity were analyzed as continuous variables in the
complete sample of 120 participants. For graphing purposes only,
we have displayed the top (N ¼ 29) and bottom (N ¼ 28) quartiles
of negative affectivity.
PSA predicts child negative affectivity after adjusting
for the effects of sociodemographic factors, obstetric
risk, and postnatal maternal psychological state. Our
findings are consistent with prior studies which found
that PSA exerted significant and persisting influences
on development that can be detected in the fetus
(DiPietro et al. 2002), infant, and child (Huizink et al.
2003; DiPietro et al. 2006; Buss et al. 2010; Davis and
Sandman 2010). These data suggest that (i) signals of
maternal psychosocial distress during the prenatal
period maybe transmitted to the fetus and have
persisting consequences for development, (ii) the fetus
appears to be more vulnerable to the effects of these
signals early in gestation, and (iii) maternal anxiety
related to pregnancy may have more profound
implications for the fetus as compared with generalized maternal anxiety.
The consequences of maternal PSA based on the
timing of exposure is consistent with prior study
evaluating the consequences of this type of psychological distress (Buitelaar et al. 2003; Huizink et al.
2003; Buss et al. 2010; Davis and Sandman 2010) and
may result from changes in PSA over gestation
(Dunkel Schetter and Glynn 2011; Sandman et al.
2011), changes in maternal and placental physiology
(Brown et al. 1996; Sandman and Davis 2010), and
variations in the sensitive periods of development of
different fetal physiological systems (Seckl and
Meaney 2006). Between the gestational ages of 8
and 16 weeks, migrating neurons form the subplate
zone, in which they arborize and branch to establish
appropriate connections with afferent neurons from
the thalamus, basal forebrain, and brainstem (Sidman
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6
M. M. Blair et al.
and Rakic 1973). Exposure to elevated maternal PSA
early in gestation may alter these early developmental
processes with consequences for child functioning.
The mechanism by which maternal psychological
distress signals are transduced to the fetus is not
known, but an interaction among the maternal
environment, placental changes, and epigenetic
programming of the fetus is likely. Variation in
concentrations of stress-sensitive hormones (placental
corticotropin-releasing hormone (CRH), cortisol)
during pregnancy predicts fetal as well as infant
behavioral neurodevelopmental outcomes (de Weerth
et al. 2003; Class et al. 2008; Ellman et al. 2008;
Bergman et al. 2010; Davis and Sandman 2010; Davis
et al. 2011). Potential mechanisms by which maternal
stress and associated increases in placental CRH and
cortisol may produce long-lasting changes in brain
function have been suggested from animal models and
may include changes in gene expression (Korosi and
Baram 2009), neurotransmitter levels (Roceri et al.
2002), adult neurogenesis (Coe et al. 2003; Fujioka
et al. 2006) as well as cell growth and survival (Roceri
et al. 2002; Van den Hove et al. 2006).
The finding that PSA predicts child outcomes when
generalized measures of distress do not maybe because
stress related to events, beliefs, or fears proximal to
pregnancy is more relevant to the pregnant woman
and, therefore, more consequential to the fetus.
Furthermore, it is plausible that pregnant women are
able to more accurately report anxiety related to
pregnancy than to more generalized concerns or
worry. In contrast to other distress measures which
evaluate stress related to generalized worry, daily
hassles, and negative mood, the PSA scale evaluates
maternal stress that is directly related to her pregnancy
including concern about the health of her baby, fear
of miscarriage, and worry about the development of
pregnancy-related medical problems. It may also be
the case that PSA is more consequential than general
anxiety because it is more dynamic over the course of
gestation. Levels of PSA are highest early and then
decline through mid-gestation.
The current study is the first to examine the
association between PSA and the development of
child temperament beyond the infancy period. The
link between negative or difficult temperament in early
childhood and adverse outcomes in later life has been
well established, underscoring the importance of this
research agenda. Children classified as having a
difficult temperament during infancy and early childhood are at risk of developing behavioral problems
(Earls and Jung 1987; Sanson et al. 1993) as well as
psychiatric conditions including eating disorders,
depression, and anxiety (Kagan et al. 1999; Schwartz
et al. 1999; Martin et al. 2000; Prior et al. 2000; De
Pauw and Mervielde 2010; Dougherty and Klein
2010) during later childhood and adolescence.
This study relied on naturally occurring variations
in maternal anxiety, rather than experimental manipulations of anxiety. It is difficult, therefore, to separate
the effects of prenatal maternal psychological state
from the consequences of other factors that might
contribute to this association such as shared genes.
However, the current findings are consistent with
studies evaluating the developmental consequences of
prenatal stress among children conceived by in vitro
fertilization who were not genetically related to their
mothers (Rice et al. 2010). In addition, the present
study relied on maternal report of both maternal
psychological state and child temperament. To reduce
the effects of biased reporting of child behavior, post
partum maternal psychological state was taken into
account in all analyses. Moreover, this study used the
Early Childhood Behavior Questionnaire which
reduces maternal bias by asking mothers to report
on specific behaviors in clearly defined situations as
opposed to making evaluative judgments about their
child’s temperament. The strength of the study is that
mother –child pairs were assessed using a prospective
longitudinal design beginning early in pregnancy
which allowed for greater resolution when examining
the programing effects of prenatal maternal psychological state on development of negative temperament
in the offspring.
Clinical and research implications
Child and adult functioning, including vulnerability to
disease, appears to be determined, in part, by the
prenatal environment (Barker 1998). The current
findings indicate that prenatal maternal psychological
state exerts programing influences on the developing
fetus with implications for more negative affective
behaviors such as sadness, frustration, and perceptual
sensitivity in early childhood. Associations were
observed in a healthy, low-risk sample of mother–
child pairs. It is plausible that more profound effects
would be observed among clinically anxious or
depressed women. Because children who have high
negative affectivity in early childhood are more likely
to develop a variety of psychological disorders later in
life, it would be beneficial for clinicians to consider
PSA when working with pregnant women. These data
are encouraging because the strongest effects on child
outcome were observed with a woman’s concerns and
fears about pregnancy, and not about generalized state
anxiety. Thus, approaches focused on cognitive
reassessment of the risks associated with pregnancy
maybe most effective at promoting the psychological
health of both mother and child. Specifically, reducing
PSA may benefit a wide range of developmental
outcomes including childhood temperament and
emotional regulation, resulting in more optimal
psychological functioning and decreased risk for
psychopathology.
Prenatal anxiety and child temperament
Acknowledgments
The work of Cheryl Crippen and Christina Canino is
gratefully acknowledged.
Declaration of interest: This research was supported by the NIH (R01 HD050662 to EPD and
NS041298 to CAS). The authors report no conflicts
of interest. The authors alone are responsible for the
content and writing of the paper.
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